Rats given 5 ppm F as FAc in drinking water were able to defluorinate the compound to a significant extent, as shown by the deposition of increased amounts of fluoride in the femurs and by the excretion of increased amounts of ionic fluoride in the urine. As expected, at least some of the FAc was converted to fluorocitrate which in turn inhibited the action of aconitase in the Krebs cycle; evidence for this was provided by the fact that citrate levels in the kidneys and in the urine were elevated. In animals acutely poisoned with intraperitoneal injections of FAc, testicular weights were decreased in proportion to the doses of FAc administered. Citrate levels in the testes were increased significantly 2 hrs after injection of FAc, were still elevated after 2 days, but were normal after 7 days; histologically demonstrable damage was evident, however. In other rats receiving a single intraperitoneal injection of FAc, histologically demonstrable damage was evident in the testes at 24 hrs, and was still to be seen 42 days later, though repair was also evident. Glycolic acid, a metabolite of FAc, did not cause testicular damage when administered to rats in amounts equimolar with doses of FAc known to cause testicular damage.